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MBBS - Year 3 > The Digestive System - Small Bowel/ Nutrition, Pancreas and GI Bleeding > Flashcards

The Digestive System - Small Bowel/ Nutrition, Pancreas and GI Bleeding Flashcards

1
Q

Developmental diseases in small bowel

A

Atresia
Stenosis
Duplications
Meckel diverticulum

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2
Q

Atresia of small bowel

A

Complete occlusion of intestinal lumen or lack of continuity of ends

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3
Q

Stenosis of small bowel

A

Stricture of the intestinal lumen secondary to incomplete intraluminal diaphragm

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3
Q

Stenosis of small bowel

A

Stricture of the intestinal lumen secondary to incomplete intraluminal diaphragm

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4
Q

Duplications of small bowel

A

Enteric cysts that may communicate w/ the intestinal lumen (most common in ileum)
May cause gastric mucosa and cause peptic ulcer

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5
Q

Meckel divertiuclum

A

Partial persistence of the vitelline duct, 60-100cm before the ileocaecal valve, w/ all layers of intestinal or gastric mucosa

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6
Q

Development issues of large intestines

A

Abnormal positioning of colon in Abdominal cavity e.g. caecum in LUQ
May give rise to volvulus

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7
Q

Pathophys of coeliac disease

A

Reaction to gliadin
Gliadin binds to enterocytes, creating a hybrid antigen to which immune system responds

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8
Q

What is gliadin

A

Protein found in the gluten of wheat, rye and barely (oats are okay)

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9
Q

Condns causing intestinal obstruction

A

Herniation
Adhesions
Volvulus
Intussusception

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10
Q

Which autoantibodies are seen in coeliac disease

A

Reticulin
Endomysial transglutaminase
Most sensitive and spp - IgA endomysial ab

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11
Q

Histology seen in coeliac disease

A

Viili disappear along the small bowel and the crypts deepen (hyperplasia)
Activated cytotoxic killer T-cell invade epithelium

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12
Q

Endoscopy findings for coeliac disease

A

Abnormally smooth gut mucosa

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13
Q

Px of coeliac - GI

A

Diarrhoea and steatorrhea
Abdo pain
Bloating
Wt loss

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14
Q

Px of coeliac - extra intestinal

A

Anaemia (malabsorption of iron and folate)
Osteoporosis - Ca and vit D malabsorption
Mouth ulcers
Dermatitis herpetiformis
Infertility

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15
Q

Px of coeliac in young children

A

Diarrhoea and/ or constipation
FTT
Vomiting
Abdo protrusion

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16
Q

Epidemiology of coeliac

A

Prevalence is 1/100
Px at any age but small peak in 1-3yrs (when first exposed to gluten)

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17
Q

Risk factors for coeliac

A

Fhx
AI disease - T1DM, thyroid disease
IgA deficiency

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18
Q

Natural hx of coeliac

A

10% of pts eventually get 1’ lymphoma if not properly treated
Osteoporosis

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19
Q

Dx of coeliac

A

Anti-tTG IgA (can also use IgG)
Endomysial ab is more spp but less sensitive
Bx via upper endoscopy to confirm dx
HLA-DQ2/8 typing if dx unclear

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20
Q

What is is necessary for accurate coeliac ix

A

Pts should stay on gluten while under ix to ensure test accuracy

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21
Q

Extra tests for coeliac

A

FBC - anaemia
LFT - may see raised transaminases
Ca and albumin (low)
DEXA
Skin bx for dermatitis herpetiformis

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22
Q

Screening for coeliac

A

1st degree relatives w/ coeliac

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23
Q

Causes of villous atrophy

A

Whipple’s
Lymphoma
Peptic duodenitis
Acid damage to duodenum

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24
Q

Mx of coeliac

A

Life-long gluten free diet
Replace micronutrients if deficient

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25
Q

Monitoring for coeliac disease

A

Annual review
DEXA 1-3yrs after dx, and at menopause (55 in men)

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26
Q

IBD

A

Infl bowel disease
Incl Crohn’s disease and ulcerative colitis

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27
Q

What is Crohn’s disease

A

Systemic disease non which ulcers and fibrosis, often w/ granulomas, affect portion of the alimentary canal

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28
Q

Crohn’s disease morphology

A

Transmural involvement (all three layers)
Ulcers on mucosa - fissures and cobble stoning
Wall is oedematous w/ narrowed lumen
Fat tends to ‘creep around’ mesentery
Increased goblet cells

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29
Q

Crohn’s disease lesions

A

Lesions are sharply demarcated from normal regions (skip lesions)
Most common site of involvement is terminal ileum

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30
Q

What are pt’s w/ CD prone to, since any portion of the gut can be involved

A

Apthae in mouth
Scleorosing cholangitis
Perianal abscesses, fistulas and fissures

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31
Q

Systemic sx seen in CD

A

Same as infl enteropathy

Arthritis
Uveitis
Erythema nodosum, pyoderma gangrenosum
If HLA-B27, ankylosing spondylitis

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32
Q

Epidemiology of IBD

A

Prevalence is 1/600 in CD and 1/1000 in UC
Bimodal onset: 15-30yrs and 60-80

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33
Q

Sx of CD

A

Diarrhoea - bloody in 25%
RLQ pain
Wt loss
Fever
Fatigue

More likely to present acutely

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34
Q

Signs of CD

A

Perianal = abscesses, fistula, tags
RIF mass from infl of terminal ileum

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35
Q

Hepatobilary signs of CD

A

Gallstones
C/c hepatitis, NAFLD and cirrhosis

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36
Q

Risk factors for CD

A

Smoking
Fhx
NOD2 mutation
Caucasians

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37
Q

Ix for IBD - blood’s

A

Increased CRP/ ESR, platelets (low albumin)
Anaemia
LFT for associated hepatobiliary disease
U&Es for nutritional deficiencies

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38
Q

Ix for IBD - stool

A

Culture to rule out infection
Faecal calprotectin - marker of infl
C. diff - poor prognostic marker

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39
Q

Endoscopy for CD

A

Skip lesions
Cobblestoning appearance
Apthous ulcers
Bx - transmural disease w/ granulomas

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40
Q

Small bowel enema - radiological findings for CD

A

Strictures - Kantor’s string sign
Rose thorn ulcers
Proximal bowel dilation

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41
Q

Complications of IBD

A

Obstruction - CD
Fistula - CD
Colorectal cancer - higher in UC than CD

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42
Q

Inducing remission in CD attack

A

Methylpred IV 3/7 then pred PO 2/52
If refractory: add azathioprine or add/ switch biologic
May give enteral nutrition therapy

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43
Q

Indications for treatment for CD

A

Freq relapses
>2 steroid courses per yr
Relpase <6/52 after stopping steroids

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44
Q

Drugs for maintaining remission in CD

A

Azathioprine or mercaptopurine
May give MTX or biologics

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45
Q

Use of biologics in treating CD

A

Can be used for induction and maintenance for refractory severe disease
Examples incl infliximab or adalimumab

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46
Q

Drugs given for symptomatic relief of CD

A

Loperamide and an anti-spasmodic, but not during attacks
PPi for upper GI problems

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47
Q

Drugs given for perineal disease in CD

A

Oral metronidazole and/ or cipro
Topical mesalazine
Seton insertion for fistulae

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48
Q

Indications for surgical mx of CD

A

Needed in 70%

Medically refractory
Obstruction or perforation
Growth failure

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49
Q

What may extensive small bowel resection in CD cause

A

Short bowel syndrome

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50
Q

Features of short bowel syndrome

A

Diarrhoea
Steatorrhea
Electrolyte abnormalities
Malnutrition incl vit deficiency
Wt loss
Fatigue

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51
Q

Post-op recurrence of CD

A

30% in 1yr
Risk increased if smoker

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52
Q

Long-term surgical complications of CD procedures

A

Vit B12 deficiency, esp if >20cm removed
Bile salt malabsorption

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53
Q

Ulcerative colitis

A

IBD beginning in rectum and may extend to caeca,
Continuous pathology - NO skip lesions

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54
Q

Pathophys of UC

A

Continuous area of infl in rectum
Inflammable, friable mucosa w. crypt changes, reduced goblet cells and psuedopolyps

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55
Q

Intestinal sx of UC

A

Diarrhoea - bloody in 25%
Lower abdo cramps
Rectal sx - urgency, tenesmus

More likely to present gradually

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56
Q

Sx of UC attacks

A

Tender distended abdo
Fever
Anorexia and wt loss
May be triggered by infection

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57
Q

Non-intestinal sx of UC

A

Uveitis
Apthous ulcers (less than CD)
Clubbing
Erythema nodusum
Pyoderma gangrenous
Entero arthritis

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58
Q

Hepatobiliary sx of UC

A

PSC
C/c hepatitis, NAFLD and cirrhosis

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59
Q

Shared sx in IBD

A

Diarrhoea
Arthritis
Erythema nodosum
Pyoderma gangrenosum
Uveitis

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60
Q

Toxic megacolon

A

Complication of severe colon disease or infection - UC more likely

Bowel wall becomes paralysed due to lumen filled w/ toxins - increased release of NO, from inflamed bowel wall
Transverse colon dilation of >6cm

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61
Q

Risk factors for UC

A

Not smoking - less common in smokers
Fhx
HLA-B27

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62
Q

Endoscopy for UC

A

Sigmoidoscopy usually sufficient
Looking for mucosal granularity
Bx - crypt abscesses, loss of goblet cells

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63
Q

Mx of mild to moderate attack of UC

A

1st line - PR mesalzine if distal (descending colon, rectosigmoid) and PO if proximal
2nd line - Add pred

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64
Q

Criteria for severe attack of UC

A

> 6 stools/ day, usually bloody
Plus one of: severe, tachycardia, anaemia, ESR > 30

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65
Q

Mx of severe attack of UC

A

Admit and give IV steroids
Then ciclosporin, biologic or subtotal colectomy if refractory

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66
Q

Drugs to maintain remission in UC - mild/moderate attacks

A

Mesalazine PO +/or PR if rectosigmoid

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67
Q

Most serious complication of UC

A

Adenocarcinoma of the colon - screen w/ colonoscopy every 3yrs, starting 10yrs after dx
Colectomy is probs advisable if mucosal cells begin to look dysplastic
Cancer risk continues even if disease is quiescent, approaches 100% in 30 yrs

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68
Q

Backwash ileitis

A

Involvement of the terminal ileum in UC
Small bowel is spared

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69
Q

Drugs to maintain remission in UC - severe attacks

A

Azathioprine or mercaptopurine PO

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70
Q

Drugs given for refractory moderate-severe disease

A

Anti-TNF alpha drugs
JAK inhibitors - tofacitinib

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71
Q

Indications for surgery for UC

A

Medically-refractory c/c or a/c UC
Toxic megacolon or perforation
Dysplasia or malignancy

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72
Q

Complications of a/c surgery for UC

A

Sepsis
Poor healing due to high dose steroids

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73
Q

Complications of UC

A

Perforation
Toxic megacolon
Colorectal cancer
VTE

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74
Q

Arterial supply of cervical oesophagus

A

Inferior thyroid artery

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75
Q

Venous drainage of cervical oesophagus

A

Inferior thyroid vein

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76
Q

Arterial supply of thoracic oesophagus

A

Oesophageal branches of the thoracic aorta

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77
Q

Venous drainage of thoracic oesophagus

A

Azygous system

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78
Q

Arterial oesophagus of abdominal oesophagus

A

L gastric artery

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79
Q

Venous drainage of abdominal oesophagus

A

Portal system via L gastric vein

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80
Q

What vertebral level os the gOJ found at

A

T11

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81
Q

Blood supply of fundus

A

Short and posterior gastric branches of splenic artery

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82
Q

Blood supply of pylorus

A

Gastroduodenal artery, branch of common hepatic artery

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83
Q

Venous drainage of stomach

A

Vein run parallel to the arteries
L & R gastric arteries drain into portal venous system
The short gastric vein and the L & R gastro-omental veins drain in the superior mesenteric veins

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84
Q

What key structure is housed in the duodenum

A

Ampulla of Vater

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85
Q

Is there a clear demarcation between the jejunum and ileum

A

No
Ileum is thicker and has more ‘fatty mesentery’
Ileum contains more LNs and Peyer’s patches

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86
Q

Arterial supply of duodenum

A

Proximal to major duodenal papilla - (branches of coeliac trunk) gastroduodenal artery and superior pancreaticoduodenal artery
Distal to the major duodenal papilla - (branches of SMA) inferior pancreaticoduodenal artery

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87
Q

Arterial supply of jejunum

A

Jejunal branches of SMA

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88
Q

Arterial supply of ileum

A

Ileal branches of the SMA
Ileocolic artery supplies the distal ileum

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89
Q

Venous drainage of duodenum

A

Superior pancreaticoduodenal vein –> portal vein
Inferior pancreaticoduodenal veins —> SMV —> portal vein

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90
Q

Venous drainage of jejunum and ileum

A

SMV —> portal vein

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91
Q

Parts of the colon

A

Caecum
Ascending colon
Transverse colon
Descending
Sigmoid
Rectum
Anus

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92
Q

Arterial supply to the caecum and ascending colon

A

Midgut derived (SMA)

Ileocolic artery —> colic, anterior caecal & posterior caecal
R colic artery

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93
Q

Arterial supply to transverse colon

A

Midgut & hindgut (SMA & IMA)

R colic artery (SMA)
Middle colic artery (SMA)
L colic artery (IMA)

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94
Q

Arterial supply to descending colon

A

IMA - L colic artery

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95
Q

Arterial supply to sigmoid artery

A

Hindgut (IMA)

Sigmoid arteries, branches of IMA

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96
Q

Venous drainage of the colon

A

Mesenteric veins parallel their corresponding arteries
SMV and IMV drain their respective structures
IMV fuses w/ splenic veins, which the fins SMV to form portal vein

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97
Q

Role of SMV in venous drainage of colon

A

Drains small intestine, caeca, and ascending and transverse colon
Via jejunal, ill, ileocolic, R colic and middle colic veins

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98
Q

Role of IMV in venous drainage of colon

A

Drains descending colon through the L
Drains sigmoid via sigmoid veins
Drains rectum via superior rectal vein

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99
Q

How can we differentiate between upper and lower GI bleeding

A

Ligament of Treitz

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100
Q

Causes of upper GI bleeding

A

Peptic ulcer
Oesophageal varices
Oesohagitis
Mallory Weiss tear
Upper GI cancer
AV malformation

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101
Q

Causes of lower GI bleeding

A

Diverticulosis
Haemorrhoids
Colorectal cancer
Mesenteric ischaemia
AV malformations

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102
Q

Haematemesis

A

Vomiting fresh or altered blood

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103
Q

Malaena

A

Passage of altered (“tarry”) blood rectally

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104
Q

Haematochezia

A

Bright red rectal bleeding

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105
Q

Types of GI bleeding in relation to disease site

A

Haematemesis - proximal to ligament of Treitz
Melaena - usually upper gI
Haematochezia - usually oleo-colonic

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106
Q

Which layer do peptic ulcer usually penetrate

A

Muscularis mucosa

107
Q

Where can HP survive

A

Gastric type mucosa in the stomach (metaplastic gastric mucosa in the duodenum, oesophagus (Barrett’s))
Small bowel (Meckel’s diverticulum)

108
Q

How does HP survive in acid pH of stomach

A

Urease activity (converts urea to ammonia)
Motility
Proteases (digests protective mucus)

109
Q

How does HP damage gastric type mucosa

A

Production of ammonia - increases pH
Enzymes - proteases, lipases, mucinases

110
Q

How does NSAID use contribute to PUD

A

Causes damage to gastric epithelium topically
Causes systemic damage by inhibiting the production of prostaglandins by gasproduodenal epithelial cells

111
Q

Ddx for PUD

A

Functional dyspepsia
GORD
Biliary pain
Gastric/ duodenal malignancy
Pancreatitis
Ischaemia

112
Q

Initial assessment for peptic ulcer bleeding

A

Haemodynamic status
Risk stratification
Looking for possible causes

113
Q

Stages in mx of upper GI bleeding

A

Initial assessment - A-E
IV fluid resus and transfusion (Hb < 7)
Pt should be NBM and supplemental oxygen given
Definitive treatment
Appropriate follow-up - endoscopy once stable

114
Q

Physiological changes w/ hypovolaemia

A

Tachycardia
Peripheral shut down
Hypotension (BP may be well preserved in young and fit)
May see postural drop
Confusion
Oliguria

115
Q

Grading haemorrhagic shock

A

(Hypovolaemic shock)

Looks at blood loss, pulse, BP, RR, urine output

116
Q

Risk stratification for gI bleeidng

A

Rockall score - predicts mortality
Can be calculated pre endoscopy (max 7) or post-endoscopy (max 11)

117
Q

Glasgow-Batchford score

A

Preferred by NICE pre-endoscopy for deciding upon timing of intervention
Cut-off for intervention is >1
Parametres incl urea, Hb, SBP, pulse, tachycardia

118
Q

Timing of endoscopy following upper GI bleed

A

Dx requires endoscopy
Adequate resus required before endoscopy
Usually, 24hrs of admission

119
Q

What to do when endoscopic therapy fails for upper GI bleeding

A

Embolisation (interventional radiology)
Surgery

120
Q

When do you perform surgery for bleeding peptic ulcer

A

Minimal surgery necessary to control bleeding
Severe uncontrolled bleeding

121
Q

What constitutes as severe uncontrolled bleeding in PUD

A

After failed endoscopic pretreatment
<60y, 2nd rebleed, 8 units transfused
>60y, 1st rebleed, 4 units transfused

122
Q

Portal hypertensive bleeding

A

Spectrum of condns encompassing oesophageal, gastric and ectopic varices and portal hypertensive gastropathy

123
Q

What gradient of pressure between portal vein and iVC is needed for the devlopment of oeopshagela varices

A

10mmHg
Normal gradient is 3-7
Pressure gradient and other factors within vary wall (Laplace’s law) influence when varices bleed

124
Q

Vasoactive therapy for variceal haemorrhage

A

Examples incl terlipressin (vasopressin analogue), octreotide
Reduces splanchnic blood flow and pressures in varices

125
Q

Abx for variceal haemorrhage

A

Bacteraemia and subsequent sepsis v common
Prophylactic BSA reduce mortality - cipro, 3rd gen cephalosporin

126
Q

Secondary prevention for varicella haemorrhagew

A

Treat liver disease
Variceal obliteration
Drugs - BB
Determine cause of PHTN

127
Q

Complications of Sengstaken tube

A

Aspiration
Mucosal necrosis

128
Q

What can be done if endoscopic therapy fails for bleeding varices

A

Confirm it is variceal in origin
Balloon tamponade - sengstake tube
Portosystemic shunting

129
Q

TIPPS procedure

A

Transjugular intrahepatic portosystemic shunt
Shunts blood from portal veins to hepatic vein

‘Rescue’ therapy for refractory a/c bleeding
Definitive treatment for bleeding gastric varices

130
Q

Complications of TIPSS

A

Procedural/ technical
Infection
Stent occlusion
Rebleeding
Encephalopathy

131
Q

Structure of villi in small intestines

A

Epithelial cells in villi extend down into lamina proprietor to form crypts
Important cells reside in more protected crypts
Goblet cells produce mucous
Paneth cells produce lysosomes

132
Q

Appearance of distal jejunum on AXR

A

‘Stack of coins’
Because of valvular conniventes folds

133
Q

Segmental contraction vs peristalsis

A

Segmental contraction - mixing bile and pancreatic enzymes w/ chyme, does NOT propel the chyme
Peristalsis - advances chyme

134
Q

Different foods and peristalsis

A

Solid foods induce greater activity than liquid meals
Food high in glucose cause greater stimulation than ones high in FFA

135
Q

What is digestion

A

The breakdown of large insoluble food molecules (proteins, lipids and carbs) to small water-soluble absorbable molecules

136
Q

Production of gastric juice

A

Pepsinogen and HCl secreted into lumen
HCl converts pepsinogen to pepsin
Pepsin activates more pepsinogen, starting a chain reaction

137
Q

Proteolytic enzymes from pancreas

A

Trypsin, chymotrypsin, carboxypeptidase
Break down to peptides to AAs
RNA/ DNA to nucleotides

138
Q

Digestion of carbs

A

Salivary amylase
Pancreatic amylase
Glycoside hydrolyses e.g. maltose, sucrose
Fibre is resistant to hydrolyses and isn’t digested

139
Q

Digestion of lipids

A

Emulsifies in stomach and then in duodenum and upper small bowel with action of bile
Requires gastric lipase, pancreatic lipase, phospholipase and cholesterol esterase

140
Q

Absorption of glucose

A

Requires transport proteins, GLUT in enterocytes
Transporter binds Na and caused conformational change, moving sodium and glucose intracellularly
Na dissociates into the cytoplasm so unloaded transporter reorients back into position

141
Q

Inflow and outflow of GIT

A

IN - 2L food/fluid, 6.5-7L secretions
OUT (to recirculate) - 8.4L per day

Total loss - 100ml faeces

142
Q

Vitamins and minerals absorbed in duodenum

A

Calcium
Iron
Fat soluble vitamins - ADEK, Mg

143
Q

Vitamins and minerals absorbed in jejunum

A

Folate
Vitamin B6
Vit C
Thiamine
Niacin

144
Q

Vitamins and minerals absorbed in ileum

A

Bile slats and acids
Vit C
Vit B12 and folate
Vit D
Vit K

145
Q

Vitamins and minerals absorbed in large intetsine

A

Water
Sodium
Potassium
Chloride
Vit K
Biotin

146
Q

Intestinal failure

A

Reduction of gut function to below minimum necessary for the absorption of macronutrients and/or water & electrolytes
TPN required to maintain health

147
Q

Intestinal insufficiency

A

Reduction of gut absorptive function that does NOT require IV supplementation

148
Q

Functional classification of intestinal failure

A

Type 1 - self-limiting
Type 2 - prolonged
Type 3 - long term

149
Q

Type 1 intestinal failure

A

Post-op ileus
A/c infl

150
Q

Type 2 intestinal failure

A

GI complictaion
EC fistula
Abdominal sepsis

151
Q

Type 3 intestinal failure

A

Short bowel syndrome
C/c obstruction
Motility disorder

152
Q

5 major condns causing intestinal failure

A

Short bowel syndrome
Intestinal fistula
Intestinal dysmotility
Mechanical obstruction
Extensive small bowel mucosal disease

153
Q

Consequences of intestinal failure

A

Dehydration - treat w/ water & salt
Malnutrition - nutrition

154
Q

Treating mild intestinal failure

A

Nutrition - oral supplements, oral glucose/ saline
Water & electrolytes - dietary adjustments, NaCl

155
Q

Treating moderate intestinal failure

A

Enternal nutritiojn
Enteral electrolytes

156
Q

Treating severe intestinal failure

A

Parenteral nutrition

157
Q

Causes of short bowel syndrome

A

Massive intenstinal rescetion
Repeated intestinal resection
EC fistuale
Gastric bypass
Paediatric - intetsinal atresia, midgut volvulus

158
Q

Complications of intestinal failure

A

Dehydration
Malnutrition
Complications of IV support
Psychological
Stoma care

159
Q

Short bowel syndrome

A

Less than 2m of small bowel

160
Q

Mx of short bowel syndrome

A

St Marks solution
Double strength dioralyte
Loperamide
Codeine
Lanreotide
S/c fluids and electrolytes
IV fluids
TPN

161
Q

Intestinal failure operations

A

Reversal of stomas
Putting bowel back into continuity
Repair of fistulas
Stricturoplasty
Removal of obstruction

162
Q

Intestinal failure operations

A

Reversal of stomas
Putting bowel back into continuity
Repair of fistulas
Stricturoplasty
Removal of obstruction

163
Q

Pathophys of pancreatic cancer

A

Typically duct adenocarcinoma of the pancreatic head (80%)

164
Q

Prognosis of pancreatic cancer

A

5-yr survival is 3.3%
15% are resectable at dx
Median survival is 28-54 months

165
Q

Histology of pancreatic cancer

A

V poor vascularity
V fibrous - rich stroma in which cancer is embedded

166
Q

Risk fcators for pancreatic cancer

A

Smoking, alcohol
C/c pancreatitis
Fhx
Diabetes

167
Q

Sx of pancreatic cancer

A

B sx - wt loss, anorexia, fatigue
Worsening of DM/ new onset
Head tumours - PAINLESS obstructive jaundice (bile ducts blocked)
Body/ tail tumour - epigastric pain that radiates to back, relived leaning forward

168
Q

Signs of pancreatic cancer

A

Palpable liver, GB and/or spleen - think Courvoisier’s law
Jaundice
Ascites
Trousseau’s sign

169
Q

Courvoisier’s law

A

Palpable GB w/ jaundice is rarely gallstones, consider malignancy (pancreatic or cholangiocarcinoma)

170
Q

Trousseau’s sign of malignancy

A

Migratory thrombophlebitis and hypercoagulability
May also be seen in gastric or lung cancer

171
Q

Metastasis of pancreatic cancer

A

Presenting sx may be from mets
Commonly affects liver, lungs, peritoneum

172
Q

Referral for pancreatic cancer

A

Over 40 w/ new onset jaundice - 2WW
Over 60 w/ wt loss and any of following - CT abdo:
Diarrhoea
Back pain
N & V
Constipation
New onset DM

173
Q

Importance of cancer associated fibroblasts

A

Immunosuppressive
V dense fibrous tissue - hard for chemo to penetrate
V hypoxic enviuronment

174
Q

Ix for pancreatic cancer

A

CT - CAP
CA19.9
Bx
Bloods - FBC, LFTs, bone profile, U&Es
Endoscopic ultrasound

175
Q

General aspects of care for pancreatic cancer

A

Nutrition - PERT
Mental health
Psych support
Pain control - v important
Good palliative care

176
Q

Chemo regimes for pancreatic cancer

A

Gemcitabine and Capecitabine
FOLFIRINOX

177
Q

Surgical treatment for pancreatic cancer

A

Whipple’s procedure (Pancreaticoduodenectomy) if resectable
Biliary stent insertion by ERCP
Total pancreatectomy

178
Q

Epidemiology of a/c pancreatitis

A

Increased incidence w/ age
Common surgical emergency

179
Q

Pathogenesis of a/c pancreatitis

A

Involves intra-pancreatic activation of pancreatic enzymes and auto-digestion
Infl —> oedema, fluid shifts and hypovolaemia

180
Q

Causes of a/c pancreatitis

A

Idiopathic
Gallstones (50%)
Ethanol
Trauma
Steroids
Malignnacy and mumps
AI
Scorpion bite
Hyperlipidaemia and hyperCa
ERCP
Drugs

181
Q

Px of a/c pancreatitis

A

Sudden-onset epigastric or LUQ pain and tenderness - radiates to back, better leaning forward
N & V
SIRS
Pleural effusions and ascites if severe

182
Q

What is required for a dx of a/c pancreatitis

A

2 out of 3 of:
Typical pancreatic type pain
Increased amylase or lipase (>3x ULN)
Compatible CT, MRI or US findings

183
Q

Other causes of a raised amylase

A

Renal insufficiency
Salivary infl
Macroamylaseamia
Hereditary
Intestinal infarction/ peritonitis
Ectopic prehnancy an ovarian cyst
Appendicitis

184
Q

Bloods for a/c pancreatitis

A

FBC - increased WBC, deranged RBC (low - haemorrhage, high - dehydration)
Increased CRP
Increased LFTs
Deceased Ca if severe

185
Q

Imaging modalities for a/c pancreatitis

A

AXR
CXR
US
Abdo CT or MRCP - gold standard but only needed if dx unclear

186
Q

XR for a/c pancreatitis

A

AXR - Dilated gut (‘sentinel loop’) next to pancreas
CXR - pleural effusion

187
Q

US for a/c pancreatitis

A

May show pancreatic infl but mainly done to find gallstones
Repeat after a/c phase if gallstones found

188
Q

Drugs that may cause a/c pancreatitis

A

Azathioprine
Valproate
Thiazides
Ceratin antimicrobials - metronidaxole, sulphonamides

189
Q

Causes of pancreatic duct obstruction

A

Pnacreatic cancers
Ampullary/ periampullary cancers
Ascariasis
Duodenal cancers/ lymphomas/ mets

190
Q

What should be done for pts w/ unexplained pancreatitis

A

ALL should have a CT scan within 6/52 of dx to check no malignant ductal obstruction

191
Q

Addn sx of haemorrhagic pancreatitis

A

Bruising over both flanks (Grey-Turner’s sign)
Bruising over peri-umbilicus (Cullen’s sign)

192
Q

Glasgow score to asses severity of pancreatitis

A

PaO2 < 8 kPa
Age > 55
Neutrophilia (WBC > 15)
Ca2+ < 2mmol/L
Renal impairment (urea < 16)
Enzymes (raised LDH, AST)
Albumin < 32
Sigar (glucose) > 10mmol

> 3 is severe nd requires HDU admission

193
Q

Initial mx of a/c pancreatitis

A

Supportive care - IV fluids (catheterisation and fluid balance chart), analgesia, antiemetics, nutritional support (NG or NJ tube)
Abx if signs of infection
Mx of aetiology

194
Q

Complications of a/c pancreatitsi

A

Necrosis
Abscess formation
Peripancreatic fluid collections - seen by 2/52
Pseudocyts - 4/52
Pseudoaneurysm
VTE

195
Q

Systemic complications of a/c pancreatitis

A

ARDS
Renal failure
Shock

196
Q

Prognosis of a/c pancreatitis

A

20% mortality if severe

197
Q

Interventional treatment for a/c pancreatitis

A

Necrosectomy
Drainage of pseudocyts
If due to gallstones, offer cholecystectomy or ERCP after recovery

198
Q

What should be done for recurrent a/c pancreatitis

A

Mx of aetiology
Modify lifestyle
Consider rare causes e.g. genetic causes PSS-1, SPINK1 or AI pancreatitis (IgG4 level may be raised) - steroid responsive

199
Q

What is c/c pancreatitis characterised by

A

C/c, progressive pancreatic infl and scarring
Resulting in the loss of exocrine and endocrine function

200
Q

Most common causes of c/c pancreatitis

A

Alcohol

201
Q

A/c vs c/c pancreatitis

A

C/c is less intense and longer lastlasting
Presence of exocrine or endocrine dysfunction in c/c
Lipase / amylase is typically NOT raised in c/c

202
Q

Clinical features of c/c pancreatitis

A

Recurrent or c/c epigastric pain radiating to back
Exocrine pancreatic insufficiency —> steatorrhea and malnutrition
DM

203
Q

Ix for c/c pancreatitis

A

Blood glucose
CT (ideally) or US: pancreatic calcification

204
Q

Mx of c/c pancreatitis

A

Lifestyle - avoidance of triggers e.. smoking
Medical - pain relief, pERT
Endoscopic - relief of obstruction, stone removal, coeliac nerve block
Surgical - Whipple’s, Frey

205
Q

Diagnostic test of pancreatic exocrine insufficiency

A

Faecal elastase - low levels

206
Q

Is 2’ DM to pancreatitis common

A

No, relatively uncommon
Behaves like T1DM (destroyed islets)

207
Q

Pancreatic cancer risk and c/c pancreatitis

A

CP increases risk
Most significantly in those w/ genetic predispositions (SOPINK1) and cig smokers
No evidence for screening except in genetic group - done w/ CT abdo

208
Q

Key complications of c/c pancreatitis

A

C/c epigastric pain
Loss of exo/endocrine functions
Damage to duct system –> obstruction of excretion
Psudoecyts formation

209
Q

Risk stratification for GI bleeding

A

Rockall score - predicts mortality
Can be calculated pre endoscopy (max 7) or post-endoscopy (max 11)
Any pts w/ a score >0 erequire input

210
Q

Conservative mx of toxic megacolon

A

Bowel decompression - place pt NBM, insertion of NGT, IV fluids
Surgery indicated if pt isn’t responding to mx or develops complications

211
Q

What features constitute ‘problem drugs’ for ADR

A

Benefit-harm ratio critically balanced e.g. digoxin, anti-coag
Poor kinetics (narrow range of safety) e.g. phenytoin
Enzyme inducers/ renal effects e.g. anticonvulsant

212
Q

What features constitute ‘problem diseases/ susceptible pts’ for ADR

A

Serious consequences of therapeutic failure e.g. anti-arrythmics
Disease required multiple drugs e.g. CHF
Pt is elderly or has multiple pathology

213
Q

Examples of how mechanism of drug action predicts interactions

A

Blocked AVN conduction - bradycardia
Arterial dilatation - hypotension
CNS drugs - sedation
Antiplatelets/ anti-coag - haemorrhage
HF drugs - electrolyte abnormalities

214
Q

What to do when anticipating drug interactions

A

Monitor drug levels or response e,g, iNR
Adjust dose if interactions e.g. reduce BB if on diltiazem
Correct metabolic disturbances
Monitor when using liver enzyme inducers or inhibitors

215
Q

What effect would an enzyme inducer cause if the enzyme breaks down drugs

A

Less drug in body, less drug action

216
Q

What effect would an enzyme inhibitor cause if the enzyme breaks down drug

A

More drug in body, more drug action

217
Q

What effects would an enzyme inducer cause if the enzyme activates drugs

A

More drug in body, more drug action

218
Q

What effect would an enzyme inhibitor cause if the enzyme activates drug

A

Less drug in body, less drug action

219
Q

Oral contraceptive interactions

A

Abx
Anticonvulsants

Encouraged to use barrier method

220
Q

Abx that potentiate the effects of warfarin

A

Metronidazole
Co-trimoxazole

221
Q

Which electrolyte does ACEi increase and what problems can this cause

A

K
Significant problem if given w/ K sparing diuretics, K supplements an drugs that worsen renal function

222
Q

Alcohol and CNS drugs

A

Potentates CNS depressants
Sedating antihistanes
Benzodiazepines

223
Q

Which drug class increases alcohol conc in body

A

H2RA e.g. ranitidine

224
Q

Alcohol as a vasodilator

A

GTN and alcohol
Increased risk of hypotension & fainting
Esp when GTN used within 1hr of alcohol

225
Q

What is an ADR

A

An unfavourable outcome that occurs during or after the use of a drug

Could be:
Abnormal sign, symptom or lab tests
Any untoward or unplanned occurrence (e.g. accidental/ unwanted pregnancy)
Unexpected worsening in a concurrent illness

226
Q

What is a side effect

A

Any unintended effects
May be harmful or beneficial e..g alpha-blocker for HTN - improvement in prostatic symptoms

227
Q

When to consider ADRs - narrow benefit: harm margin

A

Limited benefit but some risk of harm e.g. HRT
Some public health measures - flu vaccines
Major benefit but substantial harm e.g. cancer chemo
Older pts - multiple comorbidities and poly pharmacy

228
Q

Reporting ADRs

A

UK Yellow Card System
Particularly important for black triangle drugs - newly launches or suspected to have sig problems

229
Q

Classification of ADR

A

Type A - dose dependent, predictable
Type b - not dose dependent, cannot be predicted pharmacologically

230
Q

Limitation of classification of ADR

A

No account of duration e.g. steroid osteoporosis - dose and length of therapy are relevant
Susceptibility - poor mobile elderly women more likely

231
Q

Examples of Type A ADR

A

BB causes bradycardia, higher dose, greater degree of bradycardia

232
Q

Examples of Type B ADR

A

Anaphylaxis to penicillin

233
Q

Monitoring and predicting ARDS

A

DoTS scheme
Dose relatedness (at what dose does ADR happen)
Time relatedness (when does it happen, should I monitor for it)
Susceptibility factors (is pt at special risk)

234
Q

Digestion and GIT - mouth

A

Ground and mixed sallivary amylase

235
Q

Digestion and GIT - stomach

A

Mixing
Acid proteases
Reservoir w/ gradual release

236
Q

Digestion and GIT - small bowel

A

Bile
Pancreatic enzymes
Absorption

237
Q

Digestion and GIT - colon

A

Water absorption
Bacterial flors
[Short chain FA, vit K]

238
Q

Is the small intestine mobile or immobile

A

Mobile - attached by mesentery to posterior abdo wall

239
Q

Features of plicae semilunaris

A

Found in jejunum
Circular folds are large, tall and closely packed in upper jejunum
Gradually reduce until lower ileum where they are absent

240
Q

Where does the blood supply of the large intestine change

A

Proximal to splenic flexure - SMA
Distal to splenic flexure - IMA

241
Q

What vertebral level is the rectum at

A

S3

242
Q

How is CT colonoscopy done

A

Cleanse bowel using laxatives
Oral contrast agent
Put pts on low residue agency
CO2 via Foley catheter PR
Scan in two positions

243
Q

Indications for imaging small bowel

A

Previous admission for SBO
Unexplained IDA [OGD & colonoscopy normal]
Malabsorption
Unexplained pain/ diarrhoea/ wt loss esp w/ raised infl markers

244
Q

Crohn’s disease radiological findings

A

Skip lesions
Ulcers
Fissures and oedema (cobble stoning)
Stenosis
Wall thickening and distortion
Fistulation
Infl mass and crypt abscesses

245
Q

Imaging suspected Crohn’s

A

Barium studies - loss of haustrations, cobble-stoning, string sign
Ultrasound - blood flow using Dopple
CT enterography - infl fat wrapping
MR enter-graphs

246
Q

Indications for imaging large bowel

A

CIBH
PR bleeding
IDA
Palpable mas
Carcinomas and polyps
Dovertoculsar
Colitis
Volvulus

247
Q

What determines the premalignant potential of polyps (adenomas)

A

Size
1cm - 10% risk of being malignant
2cm polyps - 50% risk

248
Q

Types of colitis

A

IBD - UC, Crohn’s
Ischaemia
Radiation
Infections (incl abx related)

249
Q

Imaging for suspected colon cancer

A

Colonoscopy - gold standard
Flexible sigmoidoscopy + CTC
CT CAP

250
Q

Imaging for suspected colitis

A

Rigid sigmoidoscopy
Colonoscopy
CT

251
Q

Colonoscopy vs sigmoidoscopy

A

Coloscopy looks at entire colon but sigmooidoscopy is only lower 1/3rd

252
Q

Benefits of colonoscopy over CTC

A

Able to perform biopsies

253
Q

Benefits of CTC over colonoscopy

A

Minimal prep required
Images can be reviewed after

254
Q

Anorexia

A

Reduced desire to eat

255
Q

How can we classify causes of intestinal ischaemia

A

Occlusive - thrombosis, embolus
Non-occlusive - vasoconstriction, hypoperfusion

256
Q

Colonic ischaemia vs mesenteric ischaemia

A

Colin - large intestine
Mesenteric - small intestine

257
Q

Ix for intestinal ischaemia

A

CT pelvis and abdo
Erect CXR
Echo - if source of embolism suspected
Bloods - metabolic acidosis and raised lactate
Endoscopy

258
Q

Sx of intestinal ischaemia

A

Non-spp abdo pain
Diarrhoea
Haematochezia
N & V

259
Q

Signs of intestinal ischaemia

A

Tenderness
Peritonism/ guarding
Tachycardia/ hypotension (haemodynamic instability)

260
Q

Px of c/c mesenteric ischaemia

A

Triad of:
Post-prandial abdo pain
Wt loss - food avoidance
Abdo bruit

261
Q

Mx of intestinal ischaemia - thromboembolic cause

A

Anticoagulant
Broad spectrum abx due to bacterial translocation
May need resections

262
Q

Mx of c/c mesenteric ischaemia

A

Similar to CDV mx
Reduce modifiable risk factors
Implement 2’ prevention
Revascularisation procedures may be performed

263
Q

Complications of intestinal ischaemia

A

Shock
Peritonitis
Sepsis
Necrosis
Perforation

264
Q

Barium enema findings for UC

A

Loss of haustrations
Superficial ulcerations
Psuedopolyps
In long-standing disease, colon in narrow and short - ‘drainpipe colon’

265
Q

Proctitis

A

Infl of rectum

266
Q

Does UC affect the anus

A

No

MBBS - Year 3 (9 decks)

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